Key result
KCNE1 restricts KCNQ1 voltage sensing domain movement, requiring a higher membrane potential for channel opening.
Provides mechanistic insight into how the auxiliary subunit KCNE1 modulates KCNQ1 channel gating by restricting voltage sensing domain movement.
No immediate clinical implications; leaves open translation of KCNE1-KCNQ1 gating to human arrhythmia models.
KCNQ1 is a voltage-gated K+ channel. Its gating property is dramatically changed by an auxiliary subunit KCNE1: the gating kinetics becomes almost 100 times slower and the voltage dependence (G-V curve) is shifted by +40 mV. It is still not perfectly understood how KCNE1 slows or inhibits the opening of KCNQ1 channel. Recent applications of voltage clamp fluorometry (VCF) has been elucidating many aspects of the gating in KCNQ1-KCNE1 channels. KCNE1 directly interacts with voltage sensing domain (VSD) of KCNQ1 channel and prevents VSD from going upward. As a consequence, KCNQ1-KCNE1 channels requires higher membrane potential to overcome the hindrance.
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Koichi Nakajo (2018) conducted a review in Long QT Syndrome (Basic Science). KCNE1 co-expression with KCNQ1 vs. KCNQ1 alone was evaluated on Voltage sensor domain (VSD) movement and gating kinetics. KCNE1 directly interacts with the voltage sensing domain of the KCNQ1 channel, preventing it from moving upward and requiring a higher membrane potential for channel opening.
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